{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐584, including its 5p and 3p isoforms, has emerged as a multifunctional regulator in cancer. In various malignancies—such as breast cancer where TGF‐β down‐regulates miR‐584 to elevate PHACTR1 and promote cell migration, glioma in which miR‐584 suppresses cell growth by targeting PTTG1IP or ROCK1, and thyroid cancer where it both acts as a tumor suppressor by targeting ROCK1 and, conversely, contributes to apoptosis resistance when up‐regulated by TWIST1 to inhibit TUSC2—miR‐584 modulates cell proliferation, invasion, and apoptotic processes. Its tumor‐suppressive roles have also been demonstrated in gastric cancer by down‐regulating MMP‐14, in colon cancer via interference with hnRNP A1–CDK6 interactions, in medulloblastoma by sensitizing cells to radiation/chemotherapy through HDAC1/eIF4E3 targeting, in pancreatic cancer through CCND1 inhibition, in non–small cell lung cancer (NSCLC) as evidenced by its repression via competing endogenous RNAs, in NK/T‐cell lymphoma, in sinonasal squamous cell carcinoma through regulation of FNDC3B, and in neuroblastoma via a LINC0196/miR‐584‐5p/TRIM59 axis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‐584 plays important roles in non‐malignant physiological and pathological contexts. In screens for novel tumor‐suppressor microRNAs in clear cell renal cell carcinoma and in H. pylori–transformed gastric epithelium, altered miR‐584 expression has been linked to aberrant differentiation events such as intestinal metaplasia. In the perinatal intestine, miR‐584 modulates the lactoferrin receptor post‐transcriptionally—thereby influencing nutrient absorption—while in preeclampsia, its up‐regulation in placental trophoblasts inhibits migration by targeting endothelial nitric oxide synthase (eNOS). Moreover, in hypertension, miR‐584 binds preferentially to the angiotensinogen 3′‐UTR (in an allele‐dependent manner) to down‐regulate its expression, and in coronary artery disease, lower miR‐584 levels correlate inversely with disease severity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditionally, the activity of miR‐584 is frequently regulated by competing endogenous RNA (ceRNA) networks. Circular RNAs and long non‐coding RNAs can “sponge” miR‐584—thereby relieving inhibition on downstream targets. For example, in NSCLC, circRNAs such as circABCB10 and circ_0079530 or lncRNAs like LINC00174 sequester miR‐584 to up‐regulate targets including E2F5 and RPS24, which promote tumor progression. In hepatocellular carcinoma, extracellular vesicle–derived miR‐584‐5p modulates angiogenesis through a PCK1–mediated NRF2 pathway, while in EV‐A71 infection, a hsa_circ_0045431/miR‐584/NLRP3 axis regulates inflammatory pyroptosis and viral replication."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nadège Fils-Aimé, Meiou Dai, Jimin Guo, et al. 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